Acute Stroke in the Burn Patient
Yen-Hsun Lee, MD, Chung-Lin Chen, MD, Shin-Chen Pan, MD

A 3-year-old boy was brought to our hospital with 62% TBSA burn injury by boiled water.
He received modern burn therapy, including early débridment and skin grafts. The patient
discharged 70 days after being burned. Unfortunately, he sustained an acute right-sided
hemiparesis 7 days after discharge. Magnetic resonance imaging revealed left middle cerebral artery territory infarction, and a magnetic resonance angiogram showed nonvisualization of left distal intra-cranial carotid artery and proximal middle cerebral artery. Thickened
walls of these arteries indicated acute dissection. The patient received a follow-up magnetic
resonance angiogram study 10 years later to check cerebral vascular lesions that may not
have been apparent on the original image studies. It showed only persistently thickened left
distal intra-cranial carotid artery and middle cerebral artery walls, indicative of old dissection. Therefore, carotid artery dissection must be considered as one cause of acute stroke in
pediatric burn patient, even in the recovery phase of burn injury. (J Burn Care Res 2007;
28:351–354)

The altered physiological and homeostatic responses
after burn injury make the victim susceptible to a
variety of complications. Central nervous system
complications include seizure, focal neurological deficits, and changes in consciousness and result mostly
from dehydration, hypoxia, and metabolic disturbance.1 Acute ischemic infarction in the acute phase
of burn injury also has been reported.2 However,
stroke induced by acute carotid artery dissection in
the recovery phase of burn injury has not been reported in the literature. We describe a case study of
this injury and discuss the possible etiologies.

CASE REPORT
A 3-year-old boy presented to our emergency department on January 7, 1994, with a burn injury caused
by boiling water on his trunk, both upper arms, legs,
and the dorsums of both feet. Second-degree burns

From the Division of Plastic Surgery, Department of Surgery,
School of Medicine, National Cheng Kung University, Tainan,
Taiwan R.O.C.
Address correspondence to Chung-Lin Chen, MD, Division of
Plastic Surgery, Department of Surgery, School of Medicine,
National Cheng Kung University 138 Sheng-Li Rd,
Department of Surgery, National Cheng Kung University
Hospital, Tainan, 704, Taiwan.
Copyright © 2007 by the American Burn Association.
1559-047X/2007
DOI: 10.1097/BCR.0B013E318031A220

constituted 45% TBSA, and third-degree burns constituted 17% TBSA. He received modern burn care,
including optimal fluid resuscitation, early wound débridment, and several rounds of split-thickness skin
grafting (STSG). Central venous catheters were introduced, via bilateral internal jugular veins and femoral veins, for fluid resuscitation and medication administration during the first 5 weeks. The central lines
were removed before he was transferred to the general ward from the burn center. He was discharged 70
days after the accident.
The patient returned to the emergency department
7 days later with right lower-extremity weakness. His
body temperature was increased to 38.2°C. On the
next day, he presented additional symptoms, including mouth angle deviation to the left side, loss of right
corneal reflex, and decreased power in his right trapezius muscle. A hypodense lesion was identified in
his left frontal lobe and basal ganglia under computed
tomography (CT scan). A Magnetic resonance imaging (MRI) study showed high signal in T1-weighted
views and low signal in T2-weighted views of the left
basal ganglia and frontal areas (Figure 1). These pictures confirmed left middle cerebral artery (MCA)
territory infarction. The use of magnetic resonance
angiography (MRA) demonstrated nonvisualization
of the left internal carotid artery and branches of the
MCA. Other laboratory examinations were normal.
No cardiac anomalies were found under echocardiography, and carotid duplex confirmed the absence of
351

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March/April 2007

352 Lee et al

Figure 1. Magnetic resonance imaging shows increased signal on T2W image (A), compatible with acute ischemic infarction.
The left intra-cranial carotid artery and middle cerebral artery are absent from the magnetic resonance angiography image (B).

thrombi or vegetations in bilateral extracranial carotid arteries. The patient had normal platelet number, a normal prothrombin time, and a normal partial
thromboplastin time. He had neither bleeding problems during the acute burn period nor a family history
of autoimmune diseases. The antinuclear antibody
(ANA) titer was normal (1:40), and the protein C
level also was in the normal range. The patient’ family
refused to pay for protein S and anti-throbimIII examinations by themselves. The patient was discharged 18 days after admission when his condition
was stabilized. He has been under regular follow-up
at our out patient clinic.
Ten years later, the patient leads a normal life except sustaining grade IV/V muscle power (Medical
Research Council grading system) on his right forearm and hand. He underwent another brain MRI

examination to rule out brain lesions that may not be
apparent in its early stage. The MRI showed left MCA
territory old infarction. The thickened wall of the
distal intra-cranial carotid artery (ICA) and proximal
MCA indicates old ICA dissection (Figure 2). There
is no evidence of other vascular tumors, including
Moyamoya-like lesions, in his brain.

DISCUSSION
Antoon, Andreasen, and Sevitt in the 1970s observed
that some patients presented with neurological dysfunction after burn injury. They termed this phenomenon “burn encephalopathy” because the
causes leading to the condition were still obscure at
that time.1,3,4 Later hypoxia, hypovolemia, metabolic disturbances, infection, and vascular diseases

Figure 2. Magnetic resonance imaging 10 years after the tragedy shows the thickened wall of the left intra-cranial carotid artery
(A, arrow), evidence of organization of previous thrombus formation. Magnetic resonance angiography reveals a small vessel
indicating recanalization of left intra-cranial carotid artery and middle cerebral artery (MCA), but no branches from MCA can
be seen. A collateral artery could be seen from the dural artery in the left MCA territory (B).

Journal of Burn Care & Research
Volume 28, Number 2

were reported to be the inducing factors of burn
encephalopathy.3 Shahar et al2 reported a 13
month-old girl suffering from acute ischemic infarction in the acute phase of burn injury. However, a report of brain infarction during the recovery phase of burn injury in children has not
appeared in the literature before. Moreover, the
relation between these two devastating events has
never been discussed, either.
The reported incidence of stroke in children is approximately 7 per 100,000 children per year.5 Pediatric stroke often is multifactorial.6 The MRA examinations performed in search for the risk factors for
stroke in this 3-year-old boy revealed only distal ICA
and MCA occlusion. The MRI also demonstrated
thickening of the wall of the distal ICA. These findings
raised the initial suspicions of ICA dissection, vasculitis,
or Moyamoya disease. Ten years later, the repeat MRI
revealed no Moyamoya-like vascular collaterals or other
vascular lesions. Persistently thickened walls of the distal
ICA and MCA were noted, compatible with the previous image suggestive of vessel wall dissection. Given
that the patient suffered only one episode of stroke, it
would appear that the disease process is not progressive. We checked the protein C level for possible hereditary hypercoagulable state and serum ANA to rule
out autoimmune disease. To further clarify his coagulable status, protein S and antithrombin III levels
should be examined. For his normal platelet number,
normal prothrombin time, partial thromboplastin
time, protein C, and absent past history of bleeding
tendency as well as the normal ANA level, coagulopathy or autoimmune diseases do not seem to be the
cause in this instance.
Stroke in children frequently is associated with the
complication of Varicella zoster. Askalan et al7 found
that 31% of the children with acute ischemic infarction have had primary varicella zoster infection in the
past year. The mechanism of varicella induced stoke is
unknown, but virus-induced vasculitis was one accepted cause.8 The mean interval between infection
and stroke onset was 5.2 months.7 Angiogaphy often
reveals focal stenosis or beading of the vessels.7,9 Although the locations of the infarction in this patient
are in the basal ganglia and the frontal lobe, but beading does not feature in his MRA. Moreover, this
3-year-old boy had not suffered a varicella infection
before the burn injury.
It is possible that central venous catheter insertion
may also induce stroke. It is reported that accidental
puncture of the carotid artery could cause thromboembolism of the intracranial arteries or carotid artery
dissection, thus inducing stroke.10,11 However, according to the previous reports, the time between

Lee et al

353

puncture of the carotid artery and the onset of neurological symptoms would be several hours to 2
days.10,11 In our case report, this patient presented
with right hemiparesis in the recovery phase of his
burn injury long after the central venous catheter had
been withdrawn. Furthermore, the dissection in this
patient was intracranial. No lesion was observed in the
extracranial carotid artery when we did a neck duplex
study. Thus, central venous catheter induced stroke is
not favored. There were neither signs of wound infection nor evidence of urinary tract infection or airway infection. The white blood cell count was not
increased. The blood cultures were negative. The cardiac and carotid ultrasonography revealed no vegetations. Thus, septic emboli causing stroke is also not
likely in this instance.
Carotid dissection in children generally is classified
into spontaneous or traumatic dissection. They account for 10% to 25% of ischemic stroke in young and
middle aged patients.12 The patient has no identifiable history of neck trauma. In spontaneous carotid
artery dissection, the intracranial arteries are involved
more often than the extracranial arteries in children.13 However, the exact cause of spontaneous carotid artery dissection in children is unknown.13
Studies in adults have suggested that certain arteriopathy and a minor precipitating event, like neck hyperextension or rotation, may cause carotid artery dissection.12,13 The patient might have had a history of
rapid neck extension or rotation that was overlooked
just before the onset of neurological symptoms.
Most cervicocerebral artery dissections are single
events. The recurrence rate of infarction is 2%
to10%.12,13 The clinical condition of this patient
and his image studies are all compatible with these
aforementioned characteristics.
Stroke in children is always multifactorial.5 A triggering event that accompanies the hypercoagulable
state may make the patient succumb to thromboembolic complications like pulmonary emobolism, deep
venous thrombsosis, and even cerebral infarction.
Anticoagulation or antiplatelet agents may be beneficial to the patient. Anticoagulant therapy has been
reported to decrease recurrence rates in patients with
cervicocerebral artery dissection.12–14 However, the
beneficial effect in burn patients with stroke is difficult to demonstrate, given the rarity of this condition.

CONCLUSION
Acute ischemic stroke is a rare complication of burn
injury, especially in the recovery phase. Numerous
etiologies have been suggested for acute ischemic
stroke. In a pediatric burn patient, carotid artery dis-

354 Lee et al

section is one possibility and must be considered as
the cause of acute stroke.
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